Guest Post: An Open Letter To Healthcare Providers

https://goo.gl/pnDVc5

Although professionally, I am a former pediatric oncology nurse practitioner, I write this letter as an individual who lives with the long-lasting impact of late effects stemming from the successful treatment of Ewing’s Sarcoma as a child in the late 1970’s.

I write because I am fortunate to be surrounded by a healthcare team comprised of individual providers who have partnered with me to optimize my health and wellbeing; providers whom I trust and respect as experts in their respective fields and who trust and respect me as an expert in me; providers who hear me because they choose to listen; providers who don’t take my questions as a professional affront, but as an opportunity; providers who acknowledge their limits and know their resources; providers who are invested in me.

I write because my healthcare experience has been for the most part exceptional, and I want others facing similar health circumstances to have what I have worked hard to cultivate among my team.

I write because I find myself wondering if that is even possible given the all too common divide that can develop within the provider-patient relationship and the seeming unwillingness of both parties to listen one to the other.

I write because of tragedies like the death of Jess Jacobs at the hands of a “not my problem” mentality found within medical education, and sadly, medicine at large. Lest we think Jess’ case is an isolated incident, consider with me Paul Kalanithi, renowned neurosurgeon and author of When Breath Becomes Air, who wrote of an encounter with a resident in the final stages of his lung cancer,

“I could see in Brad’s eyes I was not a patient, I was a problem: a box to be checked off; an obligation to me meant adding another thing to his to do list.”

Trust me, if it’s happening to the strongest of self-advocates like Jacobs and Kalanithi, it’s a systemic problem.



Could Vitamin C Be the Cure for Deadly Infections? r

https://goo.gl/ftK4Pk

"Faced with a young patient who is dying, you have to say to yourself, what else can I do?" he recalls. There was one thing he could do: order intravenous vitamin C.

Yes, vitamin C, the ubiquitous nutrient that children are encouraged to consume by eating dark leafy greens as well as citrus, peppers and other orange-hued produce. It’s well-known to prevent scurvy and help with heart function. But Marik, who is chief of the pulmonary and critical care medicine unit at Eastern Virginia Medical School, had been reading research papers that also showed some success treating sepsis patients with intravenous vitamin C—along with a steroid to reduce inflammation and thiamine to help with absorption.

More than a million Americans fall ill from severe sepsis annually, and between 28 and 50 percent of them die, according to the National Institute of General Medical Studies. Because it often requires a long hospital stay, sepsis costs U.S. hospitals about $23 billion annually. The Global Sepsis Alliance reports that sepsis kills between 6 and 8 million people each year. That's more deaths than those caused by prostate cancer, breast cancer and AIDS combined.

Given the stakes, the vitamin C treatment didn't seem so crazy. After all, Marik knew that sepsis patients often have undetectable levels of the nutrient, compared to healthy patients. Animals produce increased levels when they are stressed, but humans, thanks to a fatal mutation, are unable to make it on their own. The studies Marik read reported that replenishing vitamin C in sepsis patients could help them deal with shock and prevent organ damage. Why not give it a try?

"Most times you don't have intravenous vitamin C, but fortunately our pharmacy had a small amount," he says. "It was like the stars were aligning." He gave Hobbs a cocktail of intravenous vitamin C, hydrocortisone and thiamine, and waited. 

The next morning, Marik came in to discover Hobbs alive and already off the medication supporting her blood pressure. Her kidney function had improved. Two hours later, she was taken off a ventilator. Three days later, she went home. "You say, wow, what just happened?" Marik recalls. If the vitamin C protocol really did cure her, the consequences would be profound. Still, he thought, it might have been a fluke.

Not long after, Marik he had another patient come in seriously ill with sepsis. He tried the same protocol and had the same success. The X-rays of a third patient who came in with pneumonia and severe sepsis revealed that, one day after the protocol, his lungs were 50 percent clearer. The second day, they were 100 percent better, Marik says. 


Study links immune responses to intestinal microbes with rheumatoid arthritis

https://goo.gl/4mRu57

In patients with rheumatoid arthritis (RA), self-reactive T cell responses cause inflammation and progressive damage to synovial joints. Although genetic risk factors for RA have been identified, environmental causes are also thought to play a role in the onset of RA. Recent work suggests that the disease is initially triggered by immune responses to gut bacteria, but how autoimmunity of intestinal origin plays a role in RA-linked autoimmune responses is unclear.

A study led by Annalisa Pianta at Massachusetts General Hospital describes two proteins derived from common types of gut bacteria that evoke immune responses in RA patients. N-acetyl-glucosamine-6-sulfatase (GNS) and filamin A (FLNA) were identified as autoantigens that produce responses from both T and B cells in over 50% of RA patients, but not healthy controls or patients with other rheumatic diseases. Although GNS and FLNA antigens were discovered in the synovial joint fluid in RA-affected joints, GNS and FLNA proteins show remarkable similarity to proteins produced by common classes of intestinal bacteria.

It is still unclear how abnormal immune responses to gut bacteria develop and transition to autoimmune destruction of joints in RA patients. However, the findings of this study support the hypothesized link between intestinal and synovial autoimmunity. In addition, the specificity for GNS and FLNA autoantigens for RA provides a pathway for the development of approaches to improve diagnosis and treatment of this disease.


New hope for eczema from nitric oxide

https://goo.gl/YGwZwY

According to a latest study, there may be new avenues for treatment of eczema, a common allergic condition of the skin. According to the researchers at the University of Edinburgh, on exposure to sunlight, the skin releases a compound that can ease the symptoms of this condition.

According to lead researchers Dr Anne Astier, nitric oxide has powerful anti-inflammatory properties and could be studied as an alternative drug target. For this study the team of researchers exposed some health volunteer participants to UV light, on a small patch of skin. On testing they noted presence of nitric oxide in their blood stream as a result of this exposure. Nitric oxide in turn was noted to activate some specialized immune cells called the regulatory T cells. These cells kill the hyperactive inflammatory responses that lead to the symptoms of eczema in the first place.

The team of researchers noted that after light therapy eczema patients had a marked increase in the number of regulatory T cells in their blood. This also correlated directly with the improvement of the eczema symptoms and disease improvement.


A text message helped one of my patients stay in control of his health. Here’s how

https://goo.gl/mZJ6P2

One of my first patients in the inpatient medicine unit was a what we call a “bounce-back.” He had been in the hospital two or three days before with severe blood clots in his legs. During that first trip to the hospital, his doctor put him on blood thinners to prevent new clots, which can be deadly if they dislodge and get caught in the lungs. His doctor discharged him with a prescription for an anticoagulant that he was supposed to take for 90 days.

A few days later, he came back to the hospital with severe breathing problems — the clots had traveled to his lungs. When he was stable, I asked him why he didn’t take the medication his previous doctor prescribed. He told me that when he went to the pharmacy to pick it up, he learned his insurance wouldn’t cover it. He could not afford to pay out of pocket.

I empathized with this patient because he was ill, but I was also frustrated — why didn’t he contact his hospital care team or primary care doctor when he encountered this obstacle? Any of a number of people could have easily prescribed him a different medication.

What went wrong? Could we have done more at the hospital to find out if his prescription was covered? Why is there no simple system doctors can tap into to check this out?

Did my patient fail to take ownership of his health and exercise some personal responsibility, or were those blood clots in his lungs a side effect of a fragmented health care system, where speed bumps (getting a new prescription) become road blocks? Either way, that hospital stay could have been avoided altogether.

At that moment, my mind raced back to my patient with the blood clots. An automated text from his pharmacy could have saved him a lot of trouble, too. His doctors could have used that information to maximize efficiency, reduce his health care costs, and help him take steps forward instead of unnecessary and preventable steps back. We could have solved a little problem before it spiraled into a big one.

About 95 percent of Americans have cellphones, and about 77 percent have smartphones. I work with a lot of patients of limited means — not all of them have cellphones, or even cellphones that receive text messages, but many of them do.

Whether they were about vitamins or vital medications, those text messages gave me a valuable an opportunity to intervene and reflect on what went right instead of lamenting what went wrong. 


New Kidney Allocation System Associated With Increased Rates Of Transplants Among Black And Hispanic Patients

https://goo.gl/qrsmJk

Before the 2014 implementation of a new kidney allocation system by the United Network for Organ Sharing, white patients were more likely than black or Hispanic patients to receive a kidney transplant. 

To determine the effect of the new allocation system on these disparities, we examined data for 179,071 transplant waiting list events in the period June 2013–September 2016, and we calculated monthly transplantation rates (34,133 patients actually received transplants). 

Implementation of the new system was associated with a narrowing of the disparities in the average monthly transplantation rates by 0.29 percentage point for blacks compared to whites and by 0.24 percentage point for Hispanics compared to whites, which resulted in both disparities becoming nonsignificant after implementation of the new system.


Medicare Advantage Associated With More Racial Disparity Than Traditional Medicare For Hospital Readmissions

https://goo.gl/aVKXsH

We compared racial disparities in thirty-day readmissions between traditional Medicare and Medicare Advantage beneficiaries who underwent one of six major surgeries in New York State in 2013. We found that Medicare Advantage was associated with greater racial disparity, compared to traditional Medicare. 

After controlling for patient, hospital, and geographic characteristics in a propensity score based approach, we found that in traditional Medicare, black patients were 33 percent more likely than white patients to be readmitted, whereas in Medicare Advantage, black patients were 64 percent more likely than white patients to be readmitted. 

Our findings suggest that the risk-reduction strategies adopted by Medicare Advantage plans have not been successful in lowering the markedly higher rate of readmission among black patients, compared to white patients.


A New Definition Of Health Equity To Guide Future Efforts And Measure Progress

https://goo.gl/RmsfTB

Where We Landed

After months of research, reflection, and consultation with some of the nation’s leaders in health disparities and health equity research and policy, we landed on the following definition:

Health equity means that everyone has a fair and just opportunity to be as healthy as possible. This requires removing obstacles to health such as poverty, discrimination, and their consequences, including powerlessness and lack of access to good jobs with fair pay, quality education and housing, safe environments, and health care.

And because we wanted to ensure accountability, we added the following:

For the purposes of measurement, health equity means reducing and ultimately eliminating disparities in health and its determinants that adversely affect excluded or marginalized groups.

Is this definition perfect? No. Does everyone need to use these exact words? Absolutely not.

A more detailed explanation of the rationale behind this definition is provided in the RWJF report, which also outlines key steps toward achieving health equity, presents principles to guide efforts and definitions of terms that often arise in discussions of health equity, and offers examples of programs and policies that are advancing health equity.

In addition to the examples highlighted in this report, there are others in the recent National Academy of Medicine report, Communities in Action: Pathways to Health Equity. It’s one of the most downloaded reports on the Academy’s website, a significant achievement just a few months after its release. The report warns that persistent health disparities pose “severe consequences” for America and calls for action to make health equity a top priority for the nation. It highlights nine communities across the United States that are taking steps to address health inequities and calls on leaders from sectors such as education, transportation, housing, planning, public health, and business to join this effort.



Anti-epilepsy drug restores normal brain activity in mild Alzheimer's disease

These seizures (especially in the memory areas of the brain) are partially responsible for the unpredictable able-unable patterns in mild ALZ....

https://goo.gl/HihTdV

In the last decade, mounting evidence has linked seizure-like activity in the brain to some of the cognitive decline seen in patients with Alzheimer's disease. Patients with Alzheimer's disease have an increased risk of epilepsy and nearly half may experience subclinical epileptic activity -- disrupted electrical activity in the brain that doesn't result in a seizure but which can be measured by electroencephalogram (EEG) or other brain scan technology.

In a recent feasibility study, clinician-scientists at Beth Israel Deaconess Medical Center (BIDMC) tested an anti-epileptic drug for its potential impact on the brain activity of patients with mild Alzheimer's disease. The team, led by Daniel Z. Press, MD, of the Berenson-Allen Center for Non-invasive Brain Stimulation at BIDMC, documented changes in patients' EEGs that suggest the drug could have a beneficial effect. The research was published in the Journal of Alzheimer's Disease.

"In the field of Alzheimer's disease research, there has been a major search for drugs to slow its progression," said Press, an Instructor of Neurology in the Cognitive Neurology Unit at BIDMC and an Associate Professor of Neurology at Harvard Medical School. "If this abnormal electrical activity is leading to more damage, then suppressing it could potentially slow the progression of the disease."

In the seven patients able to complete the study protocol successfully, Press and colleagues analyzed changes in their EEGs. (Blood flow analysis from the MRI data is still underway.) Overall, higher doses of the anti-seizure drug appeared to normalize abnormalities seen in the patients' EEG profiles. That is, researchers saw overall increases in brain wave frequencies that had been abnormally low in Alzheimer's disease patients prior to receiving the higher dose of levetiracetam, and, likewise, saw decreases in those that had been abnormally high.

"It's worth noting, we did not demonstrate any improvement in cognitive function after a single dose of medication in this study," said Press. "It's too early to use the drug widely, but we're preparing for a larger, longer study."

Parkinson’s is Partly an Autoimmune Disease

This evidence and some other studies point to a model where an abnormal protein (maybe even a normal one if there were too many of the normal protein) increases in number until it triggers inflammation and some autoimmune process. This could apply to lots of disorders and it could fluctuate over time....

https://goo.gl/PVQ8rD

First direct evidence that abnormal protein in Parkinson’s disease triggers immune response.

Researchers have found the first direct evidence that autoimmunity–in which the immune system attacks the body’s own tissues–plays a role in Parkinson’s disease, the neurodegenerative movement disorder. The findings raise the possibility that the death of neurons in Parkinson’s could be prevented by therapies that dampen the immune response.

The study, led by scientists at Columbia University Medical Center (CUMC) and the La Jolla Institute for Allergy and Immunology, was published today in Nature.

“The idea that a malfunctioning immune system contributes to Parkinson’s dates back almost 100 years,” said study co-leader David Sulzer, PhD, professor of neurobiology (in psychiatry, neurology and pharmacology) at CUMC. “But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson’s, can activate the T cells involved in autoimmune attacks.